Eosinophilic oesophagitis endotype classification by molecular, clinical, and histopathological analyses: a cross-sectional study

Shoda, Tetsuo; Wen, Ting; Aceves, Seema S.; Abonia, J. Pablo; Atkins, Dan; Bonis, Peter A; Caldwell, Julie M.; Capocelli, Kelley E.; Carpenter, Christina; Collins, Margaret H.; Dellon, Evan S.; Eby, Michael D.; Gonsalves, Nirmala; Gupta, Sandeep K.; Falk, Gary W.; Hirano, Ikuo; Menard‐Katcher, Paul; Kuhl, Jonathan; Krischer, Jeffrey P.; Leung, John; Mukkada, Vincent A.; Spergel, Jonathan M.; Trimarchi, Michael; Yang, Guang–Yu; Zimmermann, Nives; Furuta, Glenn T.; Rothenberg, Marc E.

doi:10.1016/s2468-1253(18)30096-7

Cited by 163 publications

(138 citation statements)

References 30 publications

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“…Despite extensive gene expression profiling in biopsies from EoE patients [42, 78–80], there is no reliable tissue biomarker of EoE-related fibrostenosis. Potential therapeutic targets for EoE-related fibrosis include the biological processes, signaling pathways, cytokines and factors regulating recruitment and activation of fibroblasts, production and deposition of collagen and other ECM components and tissue stiffness.…”

Section: Epithelial Contributions To Fibrosis In Eoementioning

confidence: 99%

Epithelial-stromal crosstalk and fibrosis in eosinophilic esophagitis

2018

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Eosinophilic esophagitis (EoE) is a food allergen-induced inflammatory disorder. EoE is increasingly recognized as a cause of swallowing dysfunction, food impaction and esophageal stricture. Inflammation of the esophageal mucosa involves immune cell infiltrate, reactive epithelial changes and fibroblast activation, culminating in robust tissue remodeling toward esophageal fibrosis characterized by excess collagen deposition in the subepithelial lamina propria. Fibrosis contributes to a unique mechanical property of the EoE-affected esophagus that is substantially stiffer than the normal esophagus. There is a great need to better understand the processes behind esophageal fibrosis in order to foster improved diagnostic tools and novel therapeutics for EoE-related esophageal fibrosis. In this review, we discuss the role of esophageal inflammatory microenvironment that promotes esophageal fibrosis, with specific emphasis upon cytokines-mediated functional epithelial-stromal interplays, recruitment and activation of a variety of effector cells, and tissue stiffness. We then explore the current state of clinical methodologies to detect and treat the EoE-related esophageal stricture.

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Section: Epithelial Contributions To Fibrosis In Eoementioning

confidence: 99%

Epithelial-stromal crosstalk and fibrosis in eosinophilic esophagitis

2018

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“…Substantial progress has been made using whole-genome transcript expression profiling (transcriptome) of tissue biopsy specimens from patients with EGIDs, particularly EoE. [8][9][10][11][12][13][14][15] We previously developed a molecular EoE diagnostic panel, a set of 96 informative transcripts that can distinguish, monitor, and endotype EoE 16,17 ; however, such molecular diagnostic profiles are lacking for the other EGIDs.…”

mentioning

confidence: 99%

Molecular, endoscopic, histologic, and circulating biomarker-based diagnosis of eosinophilic gastritis: Multi-site study

Shoda

Wen

Caldwell

et al. 2020

Journal of Allergy and Clinical Immunology

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Background: Eosinophilic gastritis (EG) is a clinicopathologic disorder with marked gastric eosinophilia and clinical symptoms. There is an unmet need among patients with EG for more precise diagnostic tools. Objective: We aimed to develop tissue-and blood-based diagnostic platforms for EG. Methods: Patients with EG and control subjects without EG were enrolled across 9 Consortium of Eosinophilic Gastrointestinal Disease Researchers-associated sites. An EG Diagnostic Panel (EGDP; gastric transcript subset) and EG blood biomarker panel (protein multiplex array) were analyzed. EGDP 18 scores were derived from the expression of 18 highly dysregulated genes, and blood EG scores were derived from dysregulated cytokine/chemokine levels. Results: Gastric biopsy specimens and blood samples from 185 subjects (patients with EG, n 5 74; control subjects without EG, n 5 111) were analyzed. The EGDP (1) identified patients with active EG (P < .0001, area under the curve > _ 0.95), (2) effectively monitored disease activity in longitudinal samples (P 5 .0078), (3) highly correlated in same-patient samples (antrum vs body, r 5 0.85, P < .0001), and (4) inversely correlated with gastric peak eosinophil levels (r 5 20.83, P < .0001), periglandular circumferential collars (r 5 20.73, P < .0001), and endoscopic nodularity (r 5 20.45, P < .0001). For blood-based platforms, eotaxin-3, thymus and activation-regulated chemokine, IL-5, and thymic stromal lymphopoietin levels were significantly increased. Blood EG scores (1) distinguished patients with EG from control subjects without EG (P < .0001, area under the curve > _ 0.91), (2) correlated with gastric eosinophil levels

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“…In the future, precision medicine may be able to specifically target different therapeutic regimens based on different clinical, endoscopic, and histologic characteristics of EoE; some of this work can be informed by the EoE endotypes recently described. 7…”

Section: Clinical Presentationmentioning

confidence: 99%